SIBO — Small Intestinal Bacterial Overgrowth

The theoretical gold standard for diagnosis remains a culture of fluid drawn directly from the small intestine during endoscopy, but in practice this is an invasive, costly method rarely performed routinely. The vast majority of SIBO diagnoses in clinical practice therefore rely on non-invasive breath tests — the patient drinks a glucose or lactulose solution, and hydrogen and methane concentrations in exhaled air are measured at regular intervals. A rise in these gases above a defined threshold, especially early in the test, suggests the presence of excess sugar-fermenting bacteria already in the small intestine, before it reaches the large intestine.

SIBO is rarely a disease in its own right — more often it's a consequence of another, underlying problem that weakens one of the natural mechanisms limiting bacterial numbers in the small intestine. The most common include intestinal motility disorders (e.g. in diabetes with autonomic neuropathy, systemic sclerosis, or after an acute gastrointestinal infection that damaged the migrating motor complex), anatomical changes after abdominal surgery creating intestinal "blind loops," ileocecal valve insufficiency, and reduced stomach acidity, which under normal conditions acts as a barrier limiting the number of bacteria that reach the small intestine further downstream.

This last point has direct clinical relevance, because reduced stomach acidity isn't only a consequence of disease — it can also be a side effect of treatment. Proton pump inhibitors (PPIs), among the most commonly prescribed drugs in the world and covered in more detail in our article on proton pump inhibitors, strongly and persistently reduce hydrochloric acid production, which with chronic use may weaken this natural barrier.

The mainstay of pharmacological SIBO treatment is antibiotics that act locally in the gastrointestinal tract, above all rifaximin — poorly absorbed from the digestive tract, which limits its systemic effects and side-effect profile compared with antibiotics absorbed into the bloodstream.

In clinical practice, however, treatment doesn't stop at the antibiotic itself. Because SIBO is usually the consequence of another underlying problem (motility disorders, anatomical changes, low stomach acidity), eradicating the bacteria alone without addressing the cause often leads to recurrence within a few months. A supportive — though not replacement — role can also be played by temporarily restricting fermentable carbohydrates in the diet (the low-FODMAP protocol, described in more detail in our article on the low-FODMAP diet), used more for symptom relief than as a standalone causal therapy.

SIBO is a mechanistically and clinically well-described condition, but it's also one of those topics where the label is easily overused without proper testing. Chronic bloating and digestive discomfort are worth treating as a signal to seek consultation, rather than immediately reaching for self-selected supplements "for SIBO" — especially since those exact same symptoms can have entirely different causes, and a mistargeted intervention only delays proper treatment.